紧密连接蛋白5参与围术期应激性心脏病的作用机制

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AbstractObjective：Toexplorethemechanismoftghtjuntionprotein5（Claudin-5）inperoperativestress-inducedheartdisease. Methods：AC16humancardiacmusclecellineswereculturedanddividedintoshamgroupandischaemia/reperfusioninjury（/）group. TheClaudin-5infectedwithsilentRNAockdownndadenoviusadidedintooalgoup（Ngoup）ypoxiareoxygeti（/） group，HR+Caudi-5specicalinterferingsi）groupndH/Cludin-5overexpressionadenoviuAdgoupCladin， cytochromeCreleaseandcaspase3inmousecardiactissuesand neonatalmousecardiomyocytes（NRCM）weredetectedbyWestem Blot.CardiacsectinsofWild-typeandClaudin-5Advmicewerestainedwith2，3，5-triphenyltetrazoliumchloride（TTC）.Tecardiac functionsofWild-typeandClaudin-5AdvmicewerequantitativelyanalyzedbyechocardiographicimagingResults：Theexpreionof Claudin-intartsduatedmyoadalinjuyiirodinvivOvereprioofClain-5it theapoptoticprocess，whilereduced cytochromeCreleaseandCaspase3cleavage.TTCstaining indicated thatoverexpressionof Claudin-5showdanntiapototicctCmpaedwioupftntrcarsorengoreViproedinyadial injuryafterClaudin-5overexpresionConclusion：Claudin-5showedananti-apoptoticefectonthemyocardiumandcouldcounteract myocardialI/Rinjurysuggestingthatitcouldbeusedasatherapeutictargetforperioperativestres-inducedheartdisease.

Keywordsperioperativestressiducedheardisease;tightjunctionprotein5;cyochromeC;Caspase3;mice;experimentalstudy

围术期应激性心脏病发生率、死亡率均较高，目前针对闭塞血管早期再灌注的治疗干预，如溶解疗法或经皮冠状动脉干预是有限的[1。（剩余8983字）